The signal transduction protein GlnK is required for NifL-dependent nitrogen control of nif gene expression in Klebsiella pneumoniae.

In Klebsiella pneumoniae, transcription of the nitrogen fixation (nif) genes is regulated in response to molecular oxygen or availability of fixed nitrogen by the coordinated activities of the nifA and nifL gene products. NifA is a nif-specific transcriptional activator, the activity of which is inhibited by interaction with NifL. Nitrogen control of NifL occurs at two levels: transcription of the nifLA operon is regulated by the global ntr system, and the inhibitory activity of NifL is controlled in response to fixed nitrogen by an unknown factor. K. pneumoniae synthesizes two PII-like signal transduction proteins, GlnB, which we have previously shown not to be involved in the response of NifL to fixed nitrogen, and the recently identified protein GlnK. We have now cloned the K. pneumoniae glnK gene, studied its expression, and shown that a null mutation in glnK prevents NifL from responding to the absence of fixed nitrogen, i.e., from relieving the inhibition of NifA activity. Hence, GlnK appears to be involved, directly or indirectly, in NifL-dependent regulation of nif gene expression in K. pneumoniae. Comparison of the GlnB and GlnK amino acid sequences from six species of proteobacteria identifies five residues (residues 3, 5, 52, 54, and 64) which serve to distinguish the GlnB and GlnK proteins.